Sunday, December 30, 2012

Beware of the Football

The evolution of even a single protein-coding gene is astronomically unlikely. How do I know? Because even the evolutionists unrealistically optimistic estimates show a 27 order of magnitude shortfall. And so a review paper from last year entitled “The evolutionary origin of orphan genes” attracted no little attention. Orphan genes are protein-coding genes that appear in a single species. Because they appear only once in the evolutionary tree, they must have evolved relatively rapidly and their history cannot be traced back to early evolutionary history. This means evolutionists cannot appeal quite so much to strange, unobservable and unverifiable events and processes to explain their origin. Given the 27 order of magnitude shortfall, an explanation for how protein-coding genes evolved, including mature, functional orphan genes, would be a terrific breakthrough. So did the paper actually explain “The evolutionary origin of orphan genes”? [Hint: Lucy was an evolutionist]

The review paper did not actually explain how orphans could have evolved. Rather, it assumed they evolved and explained that, given that orphans evolved, how fast they must have evolved, how they are identified, how they can help explain protein evolution, and so forth. It did, however, in passing admit to the gravity of the underlying problem:

If de novo emergence does indeed have a large role in orphan evolution, one has to explain how a new functional protein can emerge out of a previously non-coding sequence. This would seem highly unlikely a priori, particularly when one considers our current knowledge of protein evolution

Saturday, December 29, 2012

They Don’t Realize How Silly This Is

The headline says it all: “Evolution by Splicing.” Evolutionists once believed that the species arose by mutations that altered the nucleotide sequences of protein-coding genes. But these genetic differences between species do not seem to be very significant. Next evolutionists thought perhaps the differing expression levels of the genes did the job. Perhaps it was quantity rather than quality that created the species. But again the expression level differences are not so great. Now evolutionists have a new mechanism, and it is yet another example of evolution’s reliance on complexity, serendipity and misrepresentation.

As we reported recently, new research is showing that similar genes, in different species, are spliced differently. So the resulting protein products tend to differ between species.

You learned in high school biology that a gene consists of a long sequence of nucleotides—small molecules that comprise the DNA double helix. But in the higher species the nucleotides are grouped into building blocks or exons (expressed regions). So while the gene nucleotide sequences do not differ greatly between species, and while the gene expression levels also do not differ greatly between species, the exons that are used can differ. In other words, the building blocks themselves do not differ greatly, but which building blocks are used does differ. So for the same gene, you obtain a different gene product.

So now evolutionists are saying that new species can arise from changes in these building blocks. The process is called alternative splicing. Hence the headling, “Evolution by Splicing.”

But note the trend of ever increasing complexity and serendipity. Like entropy, the complexity and serendipity of evolutionary theory inexorably grows. First, it was mutations that inserted, deleted or altered the individual nucleotides that made up a gene. Next, it was mutations that altered the signals and machinery that govern the gene expression level. And now it is mutations that alter the signals that control the splicing machinery.

At each step in this progression, as evolutionists try to keep pace with the scientific results, the theory relies on increasing levels of pre constructed molecular machinery, instructions and processes. A tremendous infrastructure must be in place in order for evolution to occur.

And of course all of that infrastructure must have evolved. Once again, evolution creates evolution and what headlines, such as “Evolution by Splicing,” do not reveal is the ever increasing and quite frankly incredible levels of complexity and serendipity that evolutionary thought entails.

Unfortunately the disingenuous reporting does not stop there. Consider how Brent Graveley, professor of genetics and developmental biology at the University of Connecticut, portrayed these new findings:

These are very important papers that provide for the first time a large-scale view of the evolution of alternative splicing in vertebrates. They demonstrate how dramatically rapidly alternative splicing evolves, and suggest that it might play a role in speciation.

It would be difficult to imagine a greater misrepresentation of the science. There was nothing in the new results that demonstrates the evolution of alternative splicing, rapidly or otherwise. The misrepresentation relies on the prior, unspoken, assumption that evolution is true—that all of biology arose spontaneously as a consequence of random events such as mutations.

With that non scientific belief as his starting point, the evolutionist then reasons that the differing splicing patterns must have evolved. And since they are found in relatively similar species, those splicing differences must have evolved rapidly. So the evolutionist then arrives at the conclusion that the new findings “demonstrate how dramatically rapidly alternative splicing evolves.”

Is it any surprise then that journalists, in turn, misrepresent the science? Here is how one journalist reported the new findings:

The results suggest that differences in the ways genetic messages are spliced have played a major role in the evolution of fundamental characteristics of species.

It is yet another example of, as I explained in Science’s Blind Spot, how religion drives science. Theology is still queen of the sciences.

Friday, December 28, 2012

Ready, Set, Go

You learned in your high school biology class that genes are copied, or transcribed, and that the transcript was used by the ribosome to synthesize a protein. But how does the cell know which genes to transcribe, which form of the gene to use, and when to transcribe it? These questions are answered by various mechanisms collectively referred to as gene regulation. The DNA region upstream of a gene may have various molecules and proteins attached which influence its expression, that DNA region and the histone proteins about which it is wrapped may have methyl groups or other small groups attached to them serving as signals, once transcribed the resulting mRNA transcript may be spliced into alternate forms, the mRNA transcript can also be controlled by snippets of RNA that bind to the transcript, the speed with which the transcript is translated into a protein can be controlled at the ribosome, and so forth. It is an incredible network of signals and mechanisms controlling which genes are used, how they are used, and when they are used. Now, new research is helping to elucidate yet another mechanism which is the equivalent of a fine-control knob on the timing of the transcription process.

Gene transcription is conducted by a massive molecular machine known as RNA polymerase which, roughly translated into English, means to glue together many nucleotides to make an RNA molecule. The transcription process entails unwinding the DNA double helix, sliding along one of the strands, grabbing the correct matching nucleotide at each rung, and gluing that nucleotide to the end of the new and growing transcript.

But before this process begins the RNA polymerase machine may pause and wait for a start signal. Apparently in these cases the task at hand is not to be accomplished as soon as possible, but rather it is coordinated and synchronized with other activities. The timing of the arrival of the RNA polymerase is not sufficiently precise so it arrives a little early, and then is paused until just the right moment.

Not too surprisingly this pausing of RNA polymerase is particularly important in the embryonic development stages where the growing embryo is undergoing a massive and complex cellular choreography of events.

The new research helps to elucidate for which genes RNA polymerase is paused, and how this pausing regulation of RNA polymerase varies over time and between tissues.

It is yet another mechanism in the fantastically complex gene regulation.

No Pain, No Gain

You’ve heard of “red in tooth and claw,” natural selection, and the survival of the fittest. As one evolutionist put it, “The death of unfit individuals is what causes a species to adapt and improve.” This is because evolutionary theory is founded on that Malthusian idea of limited resources. Life is a zero-sum game. And so when a chance mutation happens to confer a reproductive advantage to one individual, he and his descendants survive and propagate at the cost of others, who do not. It is evolution’s version of a final accounting, but in this Darwinian spreadsheet there is no forgiveness, just survival. Of the fittest that is, and death of the unfit.

And if death is a necessary part of the evolutionary equation, then conflict can’t be too far behind. To wit, evolutionists are now saying that “Fighting may have shaped the evolution of the human hand.” This because they discovered that a clenched fist works pretty well when throwing a punch.

Oddly enough our evolutionary cousins, chimpanzees and bonobos don’t generally clench their firsts and may not be able to do so. Oh well, their loss was our gain. Death, or at least a good rumble, is evolution’s engine of progress.

Tuesday, December 25, 2012

What a Mess, Alternative Splicing is Not Conserved Across Different Species

Remember when evolution created all of biology one mutation at a time? That quaint idea from your high school biology class was about as likely as an alien world smashing into the Earth last Friday. But at least it had the virtue of not being circular. No such luck today as now evolution has to create itself. Call it evolvability, call it pre planned evolutionary pathways or call it just plain serendipity, it all means the same thing: Evolution must have constructed elaborate mechanisms and structures which then became crucial agents of evolution, creating all kinds of biological wonders. Simply put, evolution must have created evolution. In recent years such serendipity in the evolution narrative has skyrocketed. If it were a stock you would be a millionaire by now. And the latest IPOs are the spliceosomes and exons which, if evolution is true, must be crucial in the creation of, err, pretty much all the higher species.

You learned in your high school that genes are segments of DNA, but it is a bit more complicated than that. For starters, in the higher species a gene is often not a continuous segment of DNA but rather is interrupted several times by intervening segments. So there are the segments that make up the gene (called exons for expressed regions) and then there are the intervening segments (called introns for intervening regions).

Of course evolutionists figured that the introns were a big mistake and this genetic architecture was a big kludge. This despite the astonishingly complex spliceosome machine that removes the introns from the gene copy and glues the exons together. Evolutionists figured that evolution just happened to create and insert the supposedly worthless introns (evolutionists never could decide if the introns have been there all along or if they were inserted later in evolutionary history) and then just happened to create the fantastic spliceosome machine that just happened to know where to make the cuts to remove the introns and just happened to know how to glue the exon pieces back together.

Of course, as usual, evolutionists had to recant their just-so story as introns, while far from completely understood, are definitely not worthless. Evolutionists still insist the whole apparatus somehow evolved, though they have no idea how.

One of the features of the exon/intron genetic architecture is that it allows for alternative splicing schemes. In fact, incredibly, a given gene can have thousands of different forms depending on how the spliceosome machine edits the gene. And these alternative splicing schemes vary between tissue. In other words, the alternative splicing schemes are tissue-specific.

But new research adds yet more monumental problems for evolution, for these alternative splicing schemes are often not conserved between otherwise similar species. Evolution says that traits of different species should fall into the evolutionary tree, common descent, pattern.

Instead we now must believe that evolution not only (i) somehow created this fantastic architecture and apparatus with its spliceosomes, exons, introns and alternative splicing schemes, and evolution must have (ii) tailored those alternative splicing schemes for the different tissues, but evolution must also have (iii) changed the schemes even between similar species.

This forces evolution into yet another unlikely epicycle. Namely, those alternative splicing schemes must have been instrumental in the creation of the new species as they evolved. As one evolutionist explained:

But the core things that make a mouse a mouse may disproportionately derive from splicing patterns that differ from those of rats or other mammals.

So an important part of the evolution of a new species, such as a rat, must have been the redesign of the alternative splicing schemes. In other words, evolution occurs at the alternate splicing level. But this means that, for such evolution to occur, evolution must first have constructed the spliceosomes, exons/introns and alternative splicing architecture and apparatus.

And furthermore it means that this architecture and apparatus must have evolved in such a way that those alternative splicing schemes could easily evolve to new and different schemes which would help to create new species.

So evolution was not merely a series of random mutations accumulating and causing new species to arise. As unlikely as that is, evolution must also have created various structures which, themselves, became agents of evolution. I guess once one has come to believe that something comes from nothing then anything goes.

Saturday, December 22, 2012

And a Whole List of Other Things That Came True

Adam Sedgwick was a class act and his November 24, 1859 letter to Charles Darwin is a classic. In the 1128 word missive the aging professor of geology at Cambridge University—after reading Darwin’s massive work in less than a week amidst his many other duties—managed to pack several cogent criticisms and profound observations of evolutionary thought.

Sedgwick began his review by explaining that he had read the younger Darwin’s manuscript “with more pain than pleasure.” For while parts were admirable and other parts humorous, there nonetheless were so many passages that Sedgwick read “with absolute sorrow; because I think them utterly false & grievously mischievous.”

For Darwin, it seemed to Sedgwick, had abandoned the tried and true method of empirically-based scientific induction and substituted for it his own baseless assumptions:

Many of your wide conclusions are based upon assumptions which can neither be proved nor disproved. Why then express them in the language & arrangements of philosophical induction?

Neither proved nor disproved? What a prophecy of the evolutionary just-so stories to come.

And as for Darwin’s grand principle, natural selection, “what is it but a secondary consequence of supposed, or known, primary facts.” Yet Darwin had smuggled in teleological language to avoid the absurdity and make it acceptable. For Darwin had written of natural selection “as if it were done consciously by the selecting agent.” Yet again, this criticism is cogent today. Teleological language is rampant in the evolutionary literature.

And anticipating the fixity-of-species strawman, Sedgwick explained to the Sage of Kent that he had conflated the observable fact of change over time (development) with the explanation of how it came about. Everyone agreed on development, but the key question of its causes and mechanisms remained. Darwin had used the former as a sort of proof of a particular explanation for the latter. “We all admit development as a fact of history;” explained Sedgwick, “but how came it about?”

Again, how cogent. Even to this day evolutionists continue to trumpet the fact of evolution because moths change color or viruses mutate, as though that somehow proves the spontaneous origin of all of biology.

Now the foundation had been laid and Sedgwick was ready to make his thesis point: “There is a moral or metaphysical part of nature as well as a physical. A man who denies this is deep in the mire of folly.” Yet again what an incredible prophecy of things to come. Evolutionary thought since Darwin extrapolated wildly on his vacuous thought experiments with so many just-so stories which tell us nothing about the actual science.

But that is not all. Sedgwick continued with his observation that the life sciences (organic science) holds a unique position within the sciences because its province includes sentient creatures and all that that entails, even consciousness and morality:

Tis the crown & glory of organic science that it does thro’ final cause, link material to moral; & yet does not allow us to mingle them in our first conception of laws, & our classification of such laws whether we consider one side of nature or the other— You have ignored this link; &, if I do not mistake your meaning, you have done your best in one or two pregnant cases to break it.

Darwin had broken the sacred trust entrusted to the life scientist with his cavalier and even presumptuous conclusions. But Sedgwick, in a chilling anticipation of the coming eugenics and abortion movements, believed such ignorance could never propagate:

Were it possible (which thank God it is not) to break it, humanity in my mind, would suffer a damage that might brutalize it—& sink the human race into a lower grade of degradation than any into which it has fallen since its written records tell us of its history.

Sedgwick correctly foresaw the terrible consequences of the modern day resurrection of the Epicurean idea that something, and in fact everything, came from nothing. Humanity would suffer damage that “might brutalize it” and sink the human race “into a lower grade of degradation than any into which it has fallen.” Today we witness a never-ending road of killing and destruction.

If only Sedgwick could have read Nietzsche when the German polymath proclaimed that it was the sick, the oppressed, the broken and the weak, rather than evil men, who were the greatest threat to humanity:

Sick people are the greatest danger for healthy people. …

The invalids are the great danger to humanity: not the evil men, not the “predatory animals.” Those people who are, from the outset, failures, oppressed, broken— they are the ones, the weakest, who most undermine life among human beings, who in the most perilous way poison and question our trust in life, in humanity, in ourselves. Where can we escape it, that downcast glance with which people carry a deep sorrow, that reversed gaze of the man originally born to fail which betrays how such a man speaks to himself—that gaze which is a sigh. “I wish I could be someone else!”— that’s what this glance sighs. “But there is no hope here. I am who I am. How could I detach myself from myself? And yet—I’ve had enough of myself!”. . . On such a ground of contempt for oneself, a truly swampy ground, grows every weed, every poisonous growth, and all of them so small, so hidden, so dishonest, so sweet. Here the worms of angry and resentful feelings swarm; here the air stinks of secrets and duplicity; here are constantly spun the nets of the most malicious conspiracies—the plotting of suffering people against the successful and victorious; here the appearance of the victor is despised. And what dishonesty not to acknowledge this hatred as hatred! …

Take a look into the background of every family, every corporation, every community: everywhere you see the struggle of the sick against the healthy—a quiet struggle, for the most part …

Sedgwick’s unfortunate vision was not long in its fulfillment.

Next Sedgwick again sensed a trend that would extrapolate beyond Darwin when he warned the younger Darwin about his “tone of triumphant confidence.” If ever there was a consistent thread amongst evolutionists, aside from their metaphysics, it would be their incredible “tone of triumphant confidence” when proclaiming that the world came from nothing. The more absurd the theory, the greater the sound and fury with which it is proclaimed.

For Darwin, warned Sedgwick, had made claims well beyond the limits of science. Darwin issued truths that were not likely ever to be found anywhere “but in the fertile womb of man’s imagination.”

The fertile womb of man’s imagination. What a cogent summary of evolutionary theory. Sedgwick made more correct predictions in his short letter than all the volumes of evolutionary literature to come.

But Sedgwick would not sign off before offering his friendship and good will. It was in the “spirit of brotherly love” that Sedgwick wrote and he asked forgiveness for any sore points he may have left. Sedgwick spoke the truth as he saw it, but at the same time held no grudges.

Thursday, December 20, 2012

Another Big Failure

Although it may seem that genomes would be made up of genes, in many higher species genes constitute only a small fraction of the DNA. The remainder of the genome is full of various elements and segments, some of which seem to be of little functional importance.

Prediction

Evolution predicts that more distant species should have greater differences in their genomes. After all, species in distant limbs of the evolutionary tree likely have different evolutionary pressures and have been evolving independently for millions of years. This genome difference should be all the more obvious for DNA changes that are functionally unimportant. Such changes can accumulate independently in the different evolutionary lineages, as they go unchecked by evolution’s selection process.

When DNA changes do influence function then the prediction becomes more complicated. These DNA changes may be selected for, or against, depending on how they affect the function, and ultimately the reproductive advantage, of the organism. But for DNA segments that are not functionally constrained, the theory of evolution predicts divergence across different species. Or in other words, for functionally unconstrained DNA, similar sequences should not be found in distant species. The corollary to this prediction is that similar DNA sequences found in distant species must be functionally constrained.

Falsification

This prediction has been falsified in the many examples of functionally-unconstrained, highly similar stretches of DNA that have been discovered in otherwise distant species. For instance, thousands of so-called ultra-conserved elements (UCEs), hundreds of base pairs in length, have been found across a range of species including human, mouse, rat, dog, chicken and fish. Evolutionists were astonished to discover these highly similar DNA sequences in such distant species. In fact, across the different species some of these sequences are 100% identical. Species that are supposed to have been evolving independently for 80 million years were certainly not expected to have identical DNA segments. “I about fell off my chair,” remarked one evolutionist. [1]

Evolutionists assumed such highly preserved sequences must have an important function. But even if true, it would be difficult to see how so little sequence variation could be tolerated. The results were not what evolutionists expected, but this was just the beginning. Subsequent laboratory studies failed to reveal any phenotype effects. A variety of knockout experiments were done to determine the function of these sequences that evolution was supposed to have preserved. But in many of the regions no function could be found. One study knocked out several UCE regions, including a stretch of 731 DNA base pairs that was hypothesized to regulate a crucial gene. Evolutionists expected the knock out to result in lethality or infertility but instead found normal, healthy mice. Months of observation and a battery of tests found no abnormalities or significant differences compared to normal mice. [2] As one of the lead researchers explained:

For us, this was a really surprising result. We fully expected to demonstrate the vital role these ultraconserved elements play by showing what happens when they are missing. Instead, our knockout mice were not only viable and fertile but showed no critical abnormalities in growth, longevity, pathology, or metabolism. [3]

Another study knocked out two massive, highly conserved, DNA regions of 1.5 million and .8 million base pairs in laboratory mice and, again, the results were viable mice, indistinguishable from normal mice in every characteristic they measured, including growth, metabolic functions, longevity and overall development. [4] “We were quite amazed,” explained the lead researcher. [5]

Extensive tests have failed to find a function for many of the UCEs and these results were surprising to evolutionists. Perhaps some mysterious functions will be discovered in the future, but the years of research at this point indicate evolution’s prediction is false. The best information we have to date, and it is extensive, indicate that the genomes of distant species include highly similar and even identical stretches of DNA that otherwise are not functionally constrained.

It is worth noting that problems posed by this evidence will not all disappear even if some mysterious function is discovered in the future. Highly similar sequences in distant species, functional or not, are simply not consistent with evolution. Because such sequences are in distant species, according to evolution such sequences must date back to a very distant ancestor. In other words, these sequences not only must have important function in the extant organisms in which they are found, but they must have evolved early in the history of life, and they must have been important in a very different organism, under very different conditions.

And whatever the mysterious function is, it must be incredibly sensitive to every detail in the DNA sequence. But how could the sequence initially evolve if little or no variation is allowed? Evolution requires a functional pathway to arrive at the sequence in the first place but the highly restricted UCEs would have none. We would have to believe that functionally important stretches of DNA, hundreds of base pairs in length, just happened to form and then were preserved by evolution. The odds against this are astronomical.

Reaction

“It can’t be true” was one evolutionist’s reaction to the UCE findings in recent years. [6] The findings falsify predictions of evolution, but they are true and they have been verified independently. Some evolutionists considered the possibility of sequence armoring. That is, perhaps these highly conserved sequences are a consequence of a strong, local, resistance to mutations at certain locations in the DNA. But it is difficult to imagine how such localized DNA protection could occur, and in any case empirical observations have ruled out this explanation.

Evolutionists have also considered the possibility of functional redundancy. In this case, no deleterious effects are observed in the knockout mice because other DNA regions perform the same function as do the deleted UCE regions. But then this would not explain why the UCE are so highly conserved.

On the other hand, perhaps the deleterious effects of removing an apparently functionless UCE are observed only in subsequent generations. But again, this idea has difficulty explaining why the UCEs are so highly conserved.

Perhaps the most common hypothesis is that many of the UCEs have functions that are difficult to detect. This is certainly possible, but it raises the problem of how evolution could select for such rare sequences and subtle function.

UCEs are another example of how the theory, rather than the evidence, drives evolutionary thought. The DNA must have a function, even though myriad tests have found none. If we cannot detect the function, then there must be a problem with the tests. There must be a function which otherwise is undetectable to us. It is a perfect example of how metaphysical certainty resists falsification as Antony Flew once illustrated in his gardener parable:

Once upon a time two explorers came upon a clearing in the jungle. In the clearing were growing many flowers and many weeds. One explorer says, “Some gardener must tend this plot.” The other disagrees, “There is no gardener.” So they pitch their tents and set a watch. No gardener is ever seen. “But perhaps he is an invisible gardener.” So they set up a barbed-wire fence. They electrify it. They patrol with bloodhounds. (For they remember how H. G. Well’s The Invisible Man could be both smelt and touched though he could not be seen.) But no shrieks ever suggest that some intruder has received a shock. No movements of the wire ever betray an invisible climber. The bloodhounds never give cry. Yet still the Believer is not convinced. “But there is a gardener, invisible, intangible, insensible, to electric shocks, a gardener who has no scent and makes no sound, a gardener who comes secretly to look after the garden which he loves.” At last the Sceptic despairs, “But what remains of your original assertion? Just how does what you call an invisible, intangible, eternally elusive gardener differ from an imaginary gardener or even from no gardener at all?”

For evolutionists evidence such as the UCEs cannot pose a problem for the theory. There must be an explanation. And as in Flew's parable, sometimes evolutionists have creative explanations for why the evidence does not seem to reveal their gardener.

Tuesday, December 18, 2012

Don’t Bet Against the House

Everyone has heard of the famous DNA macromolecule where our genes reside, but less well known is its cousin, the RNA macromolecule. Two different molecular machines produce copies of DNA for two different reasons. One machine copies the entire double helix for the purpose of duplicating the genome before the cell divides into two daughter cells. The other machine merely transcribes one of the two strands in the double helix, and only for a relatively short segment. This copy, or transcript, is an RNA, not DNA, molecule. If you remember only one thing about RNA it probably is that the RNA transcript is passed to the ribosome machine which translates RNA’s string of nucleotides into a string of amino acids which will become a new protein. For many years that was thought to be the main function of RNA—to carry information like a messenger from the DNA gene to the ribosome. Now, in spite of evolutionary theory, that has all changed.

One of the first hints of a problem came when it was discovered that, in higher organisms, those all-important genes (according to evolutionary theory) comprised only a few percent of the genome. That didn’t fit very well with evolution’s gene-centric view, so consequently much of that huge non genic portion of the genome was often taken as functionless—the so-called “junk” DNA.

The next hint of a problem came when it was discovered that much of this non genic DNA was transcribed. This, it seemed, conferred to the non genic DNA a status on par with that of the genes. For if it was useless DNA, then why would it be transcribed? Again, that didn’t fit very well with evolution’s gene-centric view, so much of that massive transcription effort was “dismissed as transcriptional noise,” as a report out this week explains.

Now, the next problem is that not only is the vast majority of the genome not made up of genes, and not only is most of those non genic portions transcribed, but those non genic portions, which come in a variety of forms, inevitably seem to turn out to be functional. In fact, the whole operation is “enormously complex.”

Darwin viewed much of biology as inefficient or useless and evolutionists ever since have followed his lead. But it’s dangerous to bet against nature. From rudimentary and “vestigial” organs to “junk” DNA and transcriptional “noise,” evolutionist’s interpretations continue to need, well, reinterpretation.

Inherit the Wind Not Enough

We recently reported on Mohamed Noor’s Introduction to Genetics and Evolution course offered through Coursera, and how the Earl D. McLean Professor and Associate Chair of Biology at Duke University presented both whig history and false science in his attempt to convince students that evolution is true. It was one manipulation and fallacy after another but with the class now wrapped up we now realize we did not know just how far evolutionists would go. Perhaps we still don’t, but we do now know that there apparently is no manipulation of history that is beneath Noor, not even this howler that the evolutionist presented to his class with a straight face: Hitler believed in Intelligent Design. And alongside this gem the students also learned from Noor that Hitler was not influenced by Darwin.

Apparently the Inherit the Wind myth, which Noor referenced early in the course, was not enough. It seems evolutionists now need to expand their whiggish story telling about the history of evolutionary thought in order to prop up their scientific story telling about evolutionary theory.

Monday, December 17, 2012

Without it Life Wouldn’t Work

RecA is a DNA repair protein and new research is helping to understand how it works. As one report explains:

Previous studies have shown that in bacteria, RecA forms a filament that winds itself around a broken, single strand of DNA. Like a matchmaker trying to find a partner for an unpaired dancer, it scours the corresponding DNA strands for a sequence that will pair up perfectly with the broken strand. Once it finds the sequence, the broken strand steps in and chemically bonds to its new partner, displacing one of the unbroken strands (which eventually pairs with the other broken strand). This elaborate molecular square dance allows the cell to go back to the work of duplicating its genome. Each broken strand now is paired with an unbroken one, and uses the intact strand as a template for replication.

But how does RecA do its job so quickly? The new research elucidates how the protein rapidly slides along the DNA macromolecule. And its speed is crucial, for without it the all-important DNA repair job wouldn’t be completed. As one of the researchers explained:

We did a calculation that found that without this kind of process that we discovered, then DNA repair would be 200 times slower. So your DNA would not be repaired quickly and damage would accumulate, possibly leading to serious diseases.

Life cannot sustain DNA damage going unrepaired. What this new research shows is that not only is the elaborate DNA repair machinery necessary, but that it is equipped with an incredible high speed search capability, which also is necessary.

This means that in addition to all the other complexities that early evolution must have created, it also must have bequeathed RecA its rapid search capability.

Sunday, December 16, 2012

Not Just a Sheet of Light Sensors

New research out of Germany is helping to pinpoint details of how the mammalian retina converts incoming light into digital signals which ultimately make their way to the brain. Before the information is shipped off to the brain, however, it undergoes massive processing which, among other things, helps to extract features present in the incoming image. It is so complex that we are still a long way from understanding how it all works. The new research, as one report explains, “show that the retina is by no means as well understood as is commonly believed.” We have discussed some of the complexities of converting the incoming light into digital signals to be sent to the brain here, here and here. There is no doubt much yet to learn about this incredible image processing capability, but what we do know indicates it is profoundly sophisticated. As the report explains:

The retina in our eyes is not just a sheet of light sensors that – like a camera chip – faithfully transmits patterns of light to the brain. Rather, it performs complex computations, extracting several features from the visual stimuli, e.g., whether the light intensity at a certain place increases or decreases, in which direction a light source moves or whether there is an edge in the image. To transmit this information reliably across the optic nerve - acting as a kind of a cable - to the brain, the retina reformats it into a succession of stereotypic action potentials – it “digitizes” it.

Feature extraction is an important technology these days, with all kinds of applications. Engineers have been working hard at developing such techniques for years. As usual, nature provides examples of astonishing precision and efficiency.

Wednesday, December 12, 2012

A Textbook Example

The recent finding that the DNA packaging technology and structure, known as chromatin, is not limited to eukaryotes but is also present in archaea, and so from an evolutionary perspective must have “evolved before archaea and eukaryotes split apart—more than 2 billion years ago,” is merely the latest in a string of misadventures evolutionists have incurred ever since they stole the histones.

Histones are the hub-like proteins which (usually) serve as the hubs about which DNA is wrapped in the chromatin structure. Like a thread wrapped around a spool this design packs DNA away for storage with an incredible packing factor. Interestingly, the histone proteins are highly similar across vastly different species. Again, from an evolutionary perspective, this means they must have evolved early in evolutionary history to a very specific design. As one textbook explains:

The amino acid sequences of four histones (H2A, H2B, H3, and H4) are remarkably similar among distantly related species. For example, the sequences of histone H3 from sea urchin tissue and of H3 from calf thymus are identical except for a single amino acid, and only four amino acids are different in H3 from the garden pea and that from calf thymus. … The similarity in sequence among histones from all eukaryotes indicates that they fold into very similar three-dimensional conformations, which were optimized for histone function early in evolution in a common ancestor of all modern eukaryotes. [1]

But the new finding pushes back this evolutionary “optimization” far earlier in time. Once again, evolution’s heroics are moved to the distant past where no one can see. Early life was not simple.

And of course DNA needs to be accessed so this histone packaging is quite dynamic. It can roll or it can be removed and moved. The histones themselves have tails that stick out and are tagged with small chemical groups that influence whether the packaging is tight or unrolled. Again, early life was not simple.

But the fact that histones are so similar across a wide range of species leads to an entirely different dilemma for evolution. For from an evolutionary perspective, it means that the histones must not tolerate change very well. Here is how a leading 1994 textbook described it:

When the number of amino acid differences in a particular protein is plotted for several pairs of species against the time since the species diverged, the result is a reasonably straight line. That is, the longer the period since divergence, the larger the number of differences. … When various proteins are compared, each shows a different but characteristic rate of evolution. Since all DNA base pairs are thought to be subject to roughly the same rate of random mutation, these different rates must reflect differences in the probability that an organism with a random mutation over the given protein will survive and propagate. Changes in amino acid sequence are evidently much more harmful for some proteins than for others. From Table 6-2 we can estimate that about 6 of every 7 random amino acid changes are harmful over the long term in hemoglobin, about 29 of every 30 amino acid changes are harmful in cytochrome c, and virtually all amino acid changes are harmful in histone H4. We assume that individuals who carried such harmful mutations have been eliminated from the population by natural selection. [2]

So the reason the histone proteins are so similar, again from an evolutionary perspective, is because mutations changing those proteins could not be tolerated. This is the evolutionary prediction and here is how the next edition of that same textbook, eight years later in the year 2002, added to the discussion of the high similarity of the histone proteins:

As might be expected from their fundamental role in DNA packaging, the histones are among the most highly conserved eucaryotic proteins. For example, the amino acid sequence of histone H4 from a pea and a cow differ at only at 2 of the 102 positions. This strong evolutionary conservation suggests that the functions of histones involve nearly all of their amino acids, so that a change in any position is deleterious to the cell. This suggestion has been tested directly in yeast cells, in which it is possible to mutate a given histone gene in vitro and introduce it into the yeast genome in place of the normal gene. As might be expected, most changes in histone sequences are lethal; the few that are not lethal cause changes in the normal pattern of gene expression, as well as other abnormalities.

There was only one problem. That is false. In fact, even at the time studies had already shown that histone H4 could well tolerate many changes. It was not merely an example of evolution pointing in the wrong direction and producing yet another failed prediction. It was an all too frequent example of evolution abusing science, force-fitting results into its framework. And of course all of this became doctrine for wider consumption. As a 2001 PBS documentary stated:

Histones interact with DNA in the chromosomes, providing structural support and regulating DNA activities such as replication and RNA synthesis. Their ability to bind to DNA depends upon a particular structure and shape. Virtually all mutations impair histone's function, so almost none get through the filter of natural selection. The 103 amino acids in this protein are identical for nearly all plants and animals.

But it is not, and was not, true that “virtually all mutations impair histone’s function.” That was not science, it was dogma disguised as science. And since then the dogma has become even more obvious. As one recent paper summarized:

Furthermore, recent systematic mutagenesis studies demonstrate that, despite the extremely well conserved nature of histone residues throughout different organisms, only a few mutations on the individual residues (including nonmodiﬁable sites) bring about prominent phenotypic defects.

It is remarkable how many residues in these highly conserved proteins can be mutated and retain basic nucleosomal function. … The high level of sequence conservation of histone proteins across phyla suggests a fitness advantage of these particular amino acid sequences during evolution. Yet comprehensive analysis indicates that many histone mutations have no recognized phenotype.

In fact, even more surprising for evolutionists, many mutations actually raised the fitness level:

Surprisingly, a subset of 27 histone mutants show a higher intensity after growth (log2 ratio >+1.5) suggesting they are collectively fitter and maintain a selective advantage under glucose limitation.

It was yet another falsified evolutionary prediction, and yet another example of evolution abusing science.

Now evolutionists propose a redundancy hypothesis. Those histone mutations are well tolerated because evolution constructed a backup mechanism. Both mechanisms would have to mutate and fail before any lethal effects could be felt.

As usual, contradictory results are accommodated by patching the theory with yet more epicycles. The epicycles make the theory far more complex, and far more unlikely, if that were so possible. In this case, evolution not only struck on incredible complexity, and did so early in history (before there were eukaryotes and nucleus’s in which to pack the DNA), but the whole design now must have incorporated layers of redundancy which we haven’t even been able to figure out yet.

And all of this, evolutionists insist, must be a fact. Anyone who would so much as doubt this truth must be blackballed.

It has been one misstep after another ever since the evolutionists stole the histones. Evolution is truly a profound theory, not for what it reveals about nature, but for what it reveals about people. Religion drives science, and it matters.

Tuesday, December 11, 2012

Where the Heavy Lifting Occurs

A report today on new research out of Spain on embryonic development of zebrafish reads “From Fish to Man: Research Reveals How Fins Became Legs.” In this study evolutionists altered the expression levels of some regulatory genes resulting in deformed fins. The idea is that the deformed fin is taking its first step toward evolving into a tetrapod limb, and that this significant evolutionary transition was due not to an altered protein changing the way fins are built, but rather a change in the levels of existing proteins. As one of the researchers explained:

First, and foremost, this finding helps us to understand the power that the modification of gene expression has on shaping our bodies.

But the results are not nearly so compelling as the evolutionists believe. First, if the evolutionary interpretation of the findings is correct, this means that evolution had already constructed all the proteins and other machinery necessary to morph a fin toward a leg. That calls for quite a bit of serendipity.

Second, the evolutionary step that was observed in the experiment did change the fin, but the result was nowhere close to a leg. In fact, what seems to have been lost in the translation, but was included in Spain’s El Mundo report, was that the result was, err, lethal to the young zebrafish. After all, they could no longer swim.

Not to worry though, for as the evolutionists assure their readers, these modified gene expression levels were undoubtedly “acompañado de otros muchos cambios.” And so it is in these “other many changes” where the heavy lifting occurs, for they would morph the fin to a leg and ensure that those modified gene expression levels “no fuesen deletéreos.” It is amazing how evolution is always able to create so many changes to arrive finally at a better design.

As usual it is the theory that informs the data rather the other way around. Imagine if evolution wasn’t known to be a fact?

Saturday, December 8, 2012

Circular

Researchers at the University of Warwick have found another round of “conserved” non coding sequences, this time in the four plant species: the papaya, poplar, Arabidopsis and grape. And if the these similar DNA sequences are found in such disparate species, then the sequences must have been present in a very distant, and much simpler, common ancestor. The problem is these CNS’s are apparently rather clever. Not only do they appear to be regulating gene expression by influencing transcription factor binding, but many of the genes regulated by these sequences are themselves transcription factors. As one researcher explains:

So it’s the transcription factors that are regulating other transcription factors—which forms this idea of there being a core common network that is shared across different plant species.

So a long time ago random mutations just happened to construct a “core common network” where promoter regions controlled how transcription factors, also designed by random mutations, would regulate the expression of genes, which again were constructed by random mutations, of other transcription factors. And this “network” would then turn out to be a crucial component in all kinds of plants yet to be designed by evolution and its random mutations. It all makes perfect evolutionary sense.

You Won’t Believe These Designs

What happens when engineers look at biology? Unlike evolutionists, they see designs for all kinds of useful applications. “Biomimicry,” explains one article, “is an incredibly productive technique.”

There are the butterflies whose colorful wings arise from fine scales and ridges creating optical interference, a technology used in low-power video displays. And there is the mosquito's proboscis—its needle that we can barely feel because it is highly serrated. Now we have serrated hypodermic needles that are much less painful.

Termites build mounds that have incredible temperature control. They maintain 87 degrees with a system of vents, drawing air from the ground, which the termites open and close as needed. Now architects are using the same principles for better building designs.

The lotus plant is self-cleaning. Water rolls off its waxy leaves due to its tiny bumps which leave no room for droplets to accumulate. Dirt is picked up by the water rather than sticking to the leaf, a design now used in self-cleaning materials including windows and high-voltage power equipment.

Humpback whales have bumps on their flippers which would seem to create more drag but they actually work better, with a third less drag than smooth versions. Now you can see bumps on turbine and fan blades that are 20 percent more efficient.

The list goes on and on. The skin of sea cucumbers, which can rapidly stiffen, inspired a plastic that can switch from a stiff to a pliable state in seconds. The odd shape of the boxfish is surprisingly efficient and inspired a new automobile design. Rodents self-sharpening teeth inspired a new blade design that is self-sharpening. The amazing gecko feet, which provide strong adhesion via the weakest of forces (the van der Waals forces) inspired the Ghecko Tape and Geckskin, which can hold up 700 pound objects.

Biomimicry works not only because nature is chocked full of incredibly effective and efficient designs, but because so many of these designs are clever and non intuitive. We never would have thought of these designs. The sheer creativity evident in biology is far more striking than its incredible high functionality. Meanwhile evolutionists still can’t figure out why their theory keeps failing.

This One Looks Really Bad

You’ve heard of novel genes—genes that are found in only one species, and you’ve heard of alternative splicing—complex genes that are edited in different ways. Now put them together and on steroids, and to top it off, all in a mere unicellar algae. It’s another damage control nightmare as evolutionists again can’t figure out what went wrong.

The explosion in molecular biology in the past fifty years brought a plethora of new DNA sequence data and with it many new contradictions for evolutionists. One interesting finding was that in the higher species, genes are often interrupted multiple times. Instead of one DNA segment, those complex genes consisted of several smaller segments separated by intervening sequences.

As usual evolutionists figured it was all a mistake, the result of random mutations wreaking more havoc, this time in the higher species. As we have discussed many times, the evolutionist’s first move is always to assume that biology is a kludge, just barely functioning. It is amazing anything works at all.

Fortunately those random mutations also created exquisite molecular machines to splice the gene at just the right places and just the right times, and glue back together the right segments, omitting those useless intervening sequences. Another disaster somehow averted.

In fact, no thanks to evolutionary theory scientists discovered that those intervening sequences aren’t so useless, and that the gene segments are not only glued back together, but they can be rearranged as well. The process is referred to as alternative splicing and it rewrites the definition of a gene. It also allows for a far greater diversity of genes.

All of this was observed in the higher species, so evolutionists assumed those random mutations caused all this trouble at some point in the evolutionary history leading to those higher species.

That is, until the recent discovery that the unicellular algae, Bigelowiella natans, is an alternative splicing wizard, up there with the best of the higher organisms. It was “an unexpected finding”:

Or as one evolution admitted, these levels of alternative splicing in B. natans:

greatly exceed that seen in the model plant Arabidopsis and on par with the human cerebral cortex, unprecedented and truly remarkable for a unicellular organism. This challenges the paradigm that complex alternative splicing is a phenomenon limited to sophisticated multicellular organisms.

It also challenges the paradigm called evolution. But as usual evolutionists easily resolve the dilemma. For once again, it is all just a mistake. The observed alternative splicing is really just “noise” in the molecular machinery—splicing errors. Like a broken calculator, evolutionary theory continues to give the same answer: it’s all just “noise.” It is amazing that evolution produced anything at all.

Alternative splicing is not the only contradiction offered up by this humble organism. B. natans also surprised evolutionists with unique, novel genes. In fact it has, err, about ten thousand unique genes.

When unique genes first starting appearing in the genomic data, evolutionists figured their evolutionary cousins would be discovered in the genomes of other species. The problem was that we did not yet have sufficient genome data in hand. Surely once the genome data from more species were obtained, the cousins of those pesky unique genes would be found. Unique genes would become a thing of the past.

But once again evolutionary theory pointed in the wrong direction. In fact, as the genomic data have increased, so have the unique genes. Now we can throw another 10,000 onto the heap.

Evolution is not motivated by the science. It never was. Darwin became convinced of transmutation for religious reasons. Since then nothing has changed. Religion drives science, and it matters.

Tuesday, December 4, 2012

As the truth becomes ever more clear, so too the mythology must become ever more powerful. As we learn more, we must deny more. They once said biology was made of simple building blocks, but as this BBC video shows in pixel-level detail, that was just another myth. So now we need a new one. I don’t know what the twenty first century’s origins theory will be, but it will be called evolution.

Sunday, December 2, 2012

“Avian flight,” a new study explains, “is one of the remarkable achievements of vertebrate evolution.” Indeed, there is the “complex biotechnical architecture of avian wings,” the “magic structural wing asymmetries” so important for aeroelastic flight control, and the “extremely precise coordination of the complex wing beat motions, together with a perfect flight guidance and control performance.”

Then there are the flight muscles, sense organs and “extremely developed cerebellum” functioning as a guidance and control computer center. These “biological elements communicate with lightning speed like an autopilot as a biotechnical marvel with unimaginable precision.” As the paper concludes, “With their spectacular flight capabilities, birds are really the inimitable flight artists of nature.”

Unimaginable precision. Spectacular flight capabilities. Extremely precise coordination. How did random mutations create such marvels? Natural selection killed off the mutations that didn’t work, but otherwise was powerless to coax the miracle mutations. Evolution requires that the mutations leading to avian flight, and everything else for that matter, knew nothing of the need at hand. They were random with respect to function.

And yet, they created such wonders as avian flight. A remarkable design that our best engineers still cannot figure out. We know that it evolved, however, because evolution is a fact. And evolutionists never bluff.

Saturday, December 1, 2012

Proteins consist of a long sequence of amino acids and those amino acids are supplied by the so-called transfer RNA, or tRNA, molecules. The tRNA molecules, in turn, are loaded with the right amino acid by the so-called aminoacyl-transfer RNA synthetases, or aaRS, proteins. There are several different versions of aaRS proteins, which load the different tRNA molecules with the different kinds of amino acids. These aaRS proteins hang around the ribosome where proteins are constructed. But as I discussed in the previous post, the lysine aaRS, also known as LysRS, has an interesting dual role. Normally it hangs around the ribosome where it binds to another LysRS to form what is known as a dimer. In this dimer configuration, there is a weak binding between (i) the 207th amino acid (a serine) of one of the LysRS proteins and (ii) the 540th and 541st amino acids (a glycine and a leucine, respectively) of the other LysRS protein. The serine side chain consists of a hydroxyl group attached to a methyl group and when the 207th amino acid’s hydroxyl group is phosphorylated (the hydrogen is replaced by a phosphate group), its binding to the opposing 540th and 541st amino acids is broken. Not surprisingly this allows the serine dimer to loosen. But this is only the beginning of a series of events caused by the phosphorylation of that serine. The serine molecules move away from the ribosome, enter the cell’s nucleus, interact with a DNA transcription factor causing (i) the production of a signaling molecule, diadenosine tetraphosphate, (ii) release of one of the transcription factor’s proteins and (iii) expression of the transcription factor’s target genes. Simply put, depending on the phosphorylation state of its 207th amino acid, LysRS has two different structural and functional states. When not phosphorylated LysRS is a crucial part of the translation process, supplying lysine amino acids to tRNA molecules. When phosphorylated it regulates gene expression. This is a major problem for evolutionary theory.

The dual role of LysRS is not viewed as a challenge to evolutionary theory by evolutionists. This is not because evolutionary theory predicts or easily accommodates this finding, but rather because evolutionists assume evolution to be true to begin with, so there can be no real challenges, only unsolved research problems.

In fact, evolutionists have accepted so many contradictions and false predictions that new contradictions have little impact. Evolutionists simply make vague speculations and move on.

But the dual role of LysRS is not easily accommodated by evolutionary theory. In fact, it is a major challenge. This is because evolution calls for a gradual buildup of functionality. New designs do not simply appear out of nowhere. Instead, rudimentary capability is supposed to have slowly been refined by chance events such as DNA mutations.

This makes the evolution of molecular machinery and processes—such as proteins and protein synthesis—not likely without a multiverse to provide a near infinite number of tries.

But ignoring such problems and assuming that proteins and processes could somehow evolve, evolutionists must now believe that random mutations and natural selection simultaneously evolved LysRS for two completely different functions.

LysRS must have had rudimentary capabilities in both translation and transcription, and both capabilities must have been refined by evolution. The phosphorylation of that key serine must have just happened to arise. The transport of LysRS from nearby the ribosome to inside the cell nucleus must have just happened to arise. And the transcription functions of LysRS must have been refined.

All of this while LysRS was refining its translation function. We don’t have scientific evidence for the evolution of these designs, but the point here is that now we must imagine two such refinements, for two different functions, evolving simultaneously.

Or evolutionists could say LysRS evolved only for its translation function, and it just so happened that its design also fulfilled a crucial transcription function as well. It was a lucky strike. And so was the phosphorylation capability of the key amino acid just at times when it was needed.

Now none of this can be proved to be impossible. And perhaps all of this did occur somehow. But the science that we currently have does not indicate this. What we know at this time tells us that the evolution of biological machines, such as LysRS and its surrounding cellular context is, far from a fact. If we are looking for scientific facts to proclaim, the fact is evolution is unlikely.

Simply put, evolution either must have evolved two independent designs simultaneously in the same protein, or it must have been a two-fer, evolving the one design and getting the second for free. Either way the evidence does not bode well for evolution.

We can argue that the metaphysics requires evolution to be true. Or we can argue that all will be well in the future when evolution is vindicated by findings yet to come. But these are not scientific arguments.

From a scientific perspective, evolution is a deeply flawed idea. People believe it is true, and their beliefs should be respected. And who knows, perhaps future discoveries will point to evolution. But for now, gene sharing findings such as with LysRS continue to add yet more scientific problems for the theory.

You’ve seen those amazing multi-purpose kitchen utensils and jackknifes that perform a dozen tasks, but it is all standard fare in biology. From the DNA molecule which stores all kinds of information (you can see examples here, here, here and here) including overlapping genes, to molecules that fulfill various roles depending on the cellular context and gene sharing, biology is the model of efficiency. Call it multi-purpose design, component reuse, optimization of information density, or whatever, it is one of biology’s biggest unsung feats and last week yet another example was published.

You may remember the two key steps in protein synthesis are transcription and translation, where (i) the DNA gene is copied and (ii) the copy is used to encode a string of amino acids, respectively. What your biology teacher did not know, however, is that one of the key enzymes in translation also is part of the massive transcription choreography.

Everyone has heard of the DNA code but few understand how it works. The copy of the DNA gene, known as messenger RNA (mRNA) consists of a string of nucleotides. Those nucleotides are taken three at a time to form a sequence of three letter words, or codons. There are 64 (4^3) different codons and transfer RNA (tRNA) molecules do the reading of these codons. Different tRNA molecules recognize different codons. The magic is that on the other end of each tRNA is glued the correct type of amino acid, corresponding to the codon that that specific tRNA will recognize.

But how did the tRNA molecules come to have the right amino acid glued on? There are enzymes that carry an amino acid and, when they find the right corresponding tRNA, they glue the amino acid onto it. So it is with these enzymes, collectively known as tRNA synthetases, where the heavy lifting occurs. They implement the DNA code.

But the new research has found that the heroics do not stop there. The scientists discovered the details of how one of the tRNA synthetases, when a phosphate group is attached to the right place, undergoes a dramatic structural and functional change. No longer is it busy gluing an amino acid to the right tRNA. Instead, it moves upstream in the assembly line process and helps to regulate the transcription activity. As one of the scientists explained:

If you think about the structural changes that occur in the synthetase we looked at in the study, it’s very much like the movie Transformers, it’s a machine that changes structure and turns into another machine that can accomplish a completely different task—like from a car to a giant robot.

Of course yet another protein is responsible for attaching the phosphate group to the right place, at the right time. But that’s another story. For now, the question is how could this tRNA synthetase have come to have this dual role?

Of course the evolution of a protein, any protein, is problematic simply because successful searches are so unlikely. The fitness landscape is rugged, pitted with myriad local minima that frustrate evolutionary searches. Even by evolutionist’s own optimistic approximations it would never occur in the lifetime of the universe.

And beyond that, there is then the problem of how tRNA synthetases in particular could have evolved. For instance, their role so heavily depends on the intricate process of translation, involving so many other molecular players. To be sure simpler versions of that process can be envisioned, but even simpler versions are complex.

It is not as though a freshly minted tRNA synthetase is going to help much if some sort of translation process is not already in place. And it is even more unlikely that such a translation process would evolve without the needed tRNA synthetases to complete the choreography. Obviously evolution requires some sort of sequence of events providing a gradual build up. But beyond speculation, we have no compelling story to tell for this miracle.

But now, on top of these massive problems, we find that tRNA synthetases can, upon a low entropy phosphorylation, transform to a completely different structure and function. Imagine the serendipity involved.

After successfully navigating the problems discussed above to construct the translation process, and after having constructed protein kinases which attach phosphate groups at convenient places, evolution’s natural selection found that one of the kinases happened to phosphorylate one of the tRNA synthetases at just the right place to perform an incredible transformation operation where the newly formed molecular machine performed just the right function in the completely different process of transcription. This is simply incredible.

Now I would be delighted to learn that I’ve stupidly overlooked some straightforward and compelling evolutionary explanation for all of this. I don’t have a dog in this fight. Perhaps evolution is true, perhaps it is false, or perhaps it is somewhere in between. I don’t care and if there is a scientific explanation of how this world of biology could have spontaneously arisen then I would gladly shout it out.

But instead of explanations all I get is pushback. It’s all my fault for attacking science, we all know evolution is true, and besides god would never make viruses anyway.

It illustrates the enormous gap between evolutionists and the evidence. For evolutionists there are no problems behind the assertion that evolution is a fact. There are only research problems of how evolution occurred. Objective, scientific evaluations of how the evidence actually bears on the theory are elusive. Religion drives science, and it matters.